Background　Opiates are widely used for treatment of chronic pain. It is noteworthy that its long-term application and abuse lead to addiction, a serious public health and social problem.　Objective　To review the roles of synaptic plasticity in the development and maintenance of opioid addiction.　Content　Synaptic plasticity is one of the major cellular events in the development of drug-addiction. Structurally, synaptic plasticity involves synapse formation, pruning, redistribution, and modification, and functionally it manifests as long-term potentiation(LTP) or long-term depression(LTD) of synaptic transmission. Chronic exposure to morphine was reported to modify synapses in the ventral tegmental area, the nucleus accumbens, the prefrontal cortex, the amygdala, and the hippocampus, probably through activating cycline-dependent kinase-5, which leads to the accumulation of FosB. The enhancement of LTP in the hippocampus in morphine addicted animals is concurred with upregulation of N-methyl-D-aspartate receptors(NMDAR) and GluR2-containing α-amino-3-hydroxy-5-methyl-isoxazole propionic acid receptors(AMPAR). These molecular events could be caused by dopamine receptor activation and epigenetic modulation. Synaptic plasticity may be related to behavioral phenotypes of morphine addiction, such as, enhanced locomotion, stereotypic behaviors, and drug seeking and intake behavior.　Trend　Further investigations are warranted to clarify whether synaptic plasticity in certain brain region(s) corelates with particular behavioral aspect(s) of morphine addiction. Location-specific disruption of synaptic plasticity could be new therapeutic strategies for opioid addiction.